共刺激分子ICOS在滤泡辅助性T细胞和TH-17细胞发育过程中调节c-Maf和IL-21的表达。

The costimulatory molecule ICOS regulates the expression of c-Maf and IL-21 in the development of follicular T helper cells and TH-17 cells.

作者信息

Bauquet Aurelie T, Jin Hulin, Paterson Alison M, Mitsdoerffer Meike, Ho I-Cheng, Sharpe Arlene H, Kuchroo Vijay K

机构信息

Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Nat Immunol. 2009 Feb;10(2):167-75. doi: 10.1038/ni.1690. Epub 2008 Dec 21.

Abstract

The inducible costimulatory molecule ICOS has been suggested to be important in the development of interleukin 17 (IL-17)-producing helper T cells (T(H)-17 cells) and of follicular helper T cells (T(FH) cells). Here we show that ICOS-deficient mice had no defect in T(H)-17 differentiation but had fewer T(H)-17 cells after IL-23 stimulation and fewer T(FH) cells. We also show that T(FH) cells produced IL-17 and that T(FH) cells in ICOS-deficient mice were defective in IL-17 production. Both T(H)-17 and T(FH) cells had higher expression of the transcription factor c-Maf. Genetic loss of c-Maf resulted in a defect in IL-21 production and fewer T(H)-17 and T(FH) cells. Thus our data suggest that ICOS-induced c-Maf regulates IL-21 production that in turn regulates the expansion of T(H)-17 and T(FH) cells.

摘要

诱导性共刺激分子ICOS被认为在产生白细胞介素17(IL-17)的辅助性T细胞(T(H)-17细胞)和滤泡辅助性T细胞(T(FH)细胞)的发育中起重要作用。在此我们表明,ICOS缺陷小鼠在T(H)-17分化方面没有缺陷,但在IL-23刺激后T(H)-17细胞较少,且T(FH)细胞也较少。我们还表明,T(FH)细胞产生IL-17,且ICOS缺陷小鼠中的T(FH)细胞在IL-17产生方面存在缺陷。T(H)-17细胞和T(FH)细胞均有更高水平的转录因子c-Maf表达。c-Maf的基因缺失导致IL-21产生缺陷以及T(H)-17细胞和T(FH)细胞减少。因此,我们的数据表明,ICOS诱导的c-Maf调节IL-21的产生,而IL-21又反过来调节T(H)-17细胞和T(FH)细胞的扩增。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索